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At least 955 records · Page 53Linked to original sources
PubMed1983

Malignization of diaphyseal aclasis.

8 secondary chondrosarcomas in 7 patients with diaphyseal aclasia are reported. Effective diagnostic imaging is a key to early operative removal of the tumours. Angiography proved to be highly useful in tracing the malignant character and true extension of the lesion. Also skeletal nuclear investigations support the diagnosis. The necessity of regular checkups of all patients suffering from diaphyseal aclasia is stressed.

Adolescent↗
PubMed1983

The origins of osteochondromas and enchondromas. A histopathologic study.

Histopathologic sections of large pieces of tissue obtained from both surgical and postmortem specimens of osteochondromas and enchondromas were analyzed to elucidate the pathogenesis of these two lesions. The osteochondroma is derived from aberrant cartilaginous epiphyseal growth plate tissue, which proliferates autonomously and separates from the normal growth plate near its edge. As growth progresses, the aberrant tissue remains in a subperiosteal location, where it may either disappear through remodeling or proliferate as an early osteochondroma perpendicular to the orientation of the growth plate from which it was derived. The enchondroma also is derived from the actively proliferating cartilaginous tissue of growth plates. For unknown reasons certain groups of chondrocytes do not proceed to undergo hypertrophy and death. As a result, a column of uncalcified cartilage extends from the underside of the growth plate into the region in which all other cartilaginous tissue has been remodeled into primary bone. The bridge to the plate may either remain intact or become interrupted by normal bone. An isolated group of chondrocytes may (1) be walled off from normal tissue by lamellar bone; (2) undergo calcification and secondary osseous remodeling, either in part or in total; or (3) proliferate as an intraosseous chondroma (benign enchondroma). A similar but not identical process of enchondroma formation may occur in fibrous dysplasia of bone, systemic growth plate dysplasias similar to achondroplasia, and osteogenesis imperfecta.

Adolescent↗
PubMedDate not supplied

False popliteal aneurysm caused by exostosis of the femur.

A 45-year-old woman with a false aneurysm of the left popliteal artery caused by an exostosis of the femur is described. The patient had a tender swelling in the distal part of the thigh and a soft-tissue tumor was initially suspected. Diagnosis was made by ultrasonography, plain X-ray and angiography. The aneurysm and exostosis were resected. The literature regarding this condition is reviewed. Surgical treatment of popliteal aneurysm is recommended mainly because of the risk of occlusion of distal vessels by peripheral embolism.

Aneurysm↗
PubMedDate not supplied

Diffuse exostoses and osteomata of the external auditory canal: a report of 100 operations.

The clinical, surgical, and postoperative findings were reviewed in 84 operations for correction of bony stenosis of the external auditory canal caused by diffuse exostoses. Sixteen operations for removal of a solitary osteoma of the external auditory canal are also included in the review. The solitary osteoma is an uncommon unilateral lesion, attached to the tympanosquamous or tympanomastoid suture line, almost always in the outer half of the ear canal. Removal is indicated in most cases and may be performed through the external meatus under local anesthesia. Diffuse exostoses of the external auditory canal are common bilaterally symmetrical hyperostoses of the tympanic bone, seen predominantly in men who are ocean swimmers. Surgical correction of the bony stenosis is indicated only if the lesion is symptomatic. At the Otologic Medical Group we perform the operation postauricularly, rather than transmeatally, in order to remove the lesion completely and to avoid complications.

Adolescent↗
PubMed1982

Scanning electron microscopy of cartilage in mice with hereditary chondrodysplasia.

Mice born with hereditary, recessive chondrodysplasia (cho/cho) are dwarfed because the cartilage model upon which the endochondral osseous skeleton develops is defective. The mutant's cartilage matrix lacks cohesiveness which apparently contributes to the absence of columnar alignment of proliferating epiphyseal chondrocytes in developing tubular (long) bones. The present communication reviews our current understanding of skeletal dysplasia as it relates to defective chondrogenesis, and presents observations made with the scanning electron microscope of cellular disarray and nonuniform size and distribution of collagen fibrils which confirm the existence of a matrix defect. Autoradiographic experiments on tibial cartilage, similar to those performed on sternal cartilage, confirm the normal pattern of sulfate labeling by mutant epiphyses.

Animals↗
PubMed1981

Immunologic studies of cartilage-hair hypoplasia in the Amish.

The immunologic status of 18 Old Order Amish persons with cartilage-hair hypoplasia and 9 unaffected sibs was studied. Although none of the subjects had a history suggestive of persistent immune dysfunction, the subjects with cartilage-hair hypoplasia had significantly lower lymphocyte mitogenic and allogeneic cell stimulation responses when compared to unaffected sibs and unrelated control subjects. The abnormalities of cellular immune function found in the 18 affected subjects were similar to those reported in Finnish subjects with cartilage-hair hypoplasia.

Adolescent↗